A recent study published in PLOS Pathogens has revealed more details of the mechanism by which the bacterium Wolbachia blocks viruses in mosquito cells. Professor Scott O’Neill, Director of the World Mosquito Program, led by Australia’s Monash University, and colleagues argue that the mechanism reduces viral replication inside cells and that rapid degradation of viral RNA is involved.

What is Wolbachia?

Wolbachia is a genus of gram-negative bacteria, a group of bacteria characterised by their cell envelopes, which are composed of a thin peptidoglycan cell ball squished between an inner cytoplasmic cell membrane and a bacterial outer membrane. If you’ve ever studied biology at undergrad, you may remember that gram-negative bacteria do not retain the crystal violet stain used in the gram-staining method of bacterial differentiation.

Wolbachia infects arthropod species, and is one of the world’s most common parasitic microbes. It has been estimated that Wolbachia is possibly the most common reproductive parasite in the biosphere, with complex interactions with its various hosts. In some cases, the relationship between host and Wolbachia is mutualistic rather than parasitic.

It was previously discovered that Wolbachia can lower a mosquitoes’ ability to transmit viral diseases, such as dengue, chikungunya and Zika, to humans. Scientists are testing whether deliberately infecting mosquito populations with Wolbachia can stop the spread of these diseases. However, the precise mechanism by which Wolbachia blocks viruses in mosquitoes is unclear.

While most investigations into Wolbachia’s virus blocking mechanism have focused on mosquitoes’ response to the bacterium, O’Neill and colleagues studied the effects of Wolbachia on dengue and West Nile viruses themselves, performing a series of experiments to examine the molecular details of each stage of viral infection in Wolbachia-infected mosquito cells.

Wolbachia does not affect DENV binding or internalisation but viral RNA replication.

No evidence was found to suggest that Wolbachia inhibits the earlier stages of virus infection, in which the virus binds to the outside of the cell, and then inserts itself inside. Rather, the researchers found evidence that would suggest the bacterium inhibits replication once the dengue or West Nile virus has infiltrated a mosquito cell. This reduced replication was associated with the rapid degeneration of viral DNA. Evidence suggested that a mosquito cellular protein called XRN1 may play a key role in this process.

O’Neill and colleagues also found evidence to indicate that the virus-blocking ability of Wolbachia also depends on the initial dose of the virus and how fast it replicates. In short, slowly replicating viruses such as dengue are blocked more effectively than faster ones, like the West Nile virus.

What is Dengue fever?

Dengue fever is a mosquito-borne tropical disease caused by the dengue virus, wherein people suffer from a high fever, headache, vomiting, muscle and joint pains, and a characteristic skin rash. Symptoms typically develop between three and fourteen days after infection, and recovery usually takes two to seven days. In a few cases, the disease can develop into dengue hemorrhagic fever, resulting in blood plasma leakage, bleeding, low levels of blood platelets. In some cases, it can also develop into dengue shock syndrome, in which dangerously low blood pressure occurs. Dengue infection is increasing globally, with around 400 million people infected each year. Although further research is needed to learn more about the molecular details behind virus blocking by Wolbachia, these new findings could help inform efforts to use the bacterium to prevent spread of disease.

“We now have a better understanding of the mechanism by which Wolbachia inhibits replication of the dengue virus and leads to the degradation of viral RNA in the mosquito cell,” O’Neill explains. “This is an important step forward in deepening our understanding of the mechanistic basis of our approach to tackling the increasing global arbovirus burden.”

Image: Wolbachia is associated with reduced replication of dengue, West Nile viruses and breakdown of their RNA

]]>https://sciblogs.co.nz/news/2018/03/05/virus-blocking-bacterium-operate-mosquitoes/feed/0Shopping trolleys and superbugs: an FAQhttps://sciblogs.co.nz/infectious-thoughts/2016/10/03/shopping-trolleys-superbugs-faq/
https://sciblogs.co.nz/infectious-thoughts/2016/10/03/shopping-trolleys-superbugs-faq/#respondMon, 03 Oct 2016 10:21:51 +0000https://sciblogs.co.nz/?p=234558A story about a baby catching a life-threatening infection from a shopping trolley has made the headlines. So what was this life threatening infection, and was the trolley really to blame?

This story originally appeared in the DailyMail Australia which saw Vivienne Wardrop’s Facebook post warning other parents about shopping trolley hygiene. Her 10 month old son is currently recovering from what clearly looks like a serious illness, which his mum has narrowed down to him catching after being sat in a shopping trolley (or a cart, for any Americans reading this..). The article says the youngster had “adenovirus, rotavirus, salmonella and meningitis” so what are all those, and was the shopping trolley to blame?

Salmonella and salmonellosis

Salmonella is a family of bacteria that is divided into 2 species, S. enterica and S. bongori. S. bongori is found in cold-blooded animals, especially reptiles, but S. enterica (of which there are over 2000 different types) is found in warm-blooded animals all around the world. S. enterica can cause typhoid fever and paratyphoid fever as well as a form of food poisoning called Salmonellosis with fever, vomiting and diarrhoea. Salmonella infections can be caught by eating or handling contaminated food (including meat, cheese, eggs, milk, fruit and veggies*) or by contact with contaminated surfaces or people.

Infected people and animals shed the bacteria in their poop, and can continue to shed the bacteria for months after they have recovered from an infection. Symptoms usually appear 6-72 hours after infection, and those most at risk of severe disease are young children, the elderly, and people with compromised immune systems. According to the Ministry for Primary Industries, Salmonella is the second most common cause of bacterial food-borne illness in New Zealand, with around 1000 cases a year [pdf].

Adenovirus, rotavirus and meningitis

Adenovirus is a virus that rarely causes severe illness although it can be a problem for infants and people with weakened immune systems. It most commonly causes respiratory symptoms, but can also cause diarrhoea and fever, usually 2-14 days after infection. The virus is spread though close contact, coughing and sneezing and touching contaminated surfaces. This is another one that can be shed by people in their poop, again for months after they’ve recovered.

Rotavirus is a really common virus which causes vomiting and diarrhoea, again spread though contaminated poop, with symptoms appearing 1-2 days after infection. 90% of NZ kids will have had a rotavirus infection by the time they are 3, and a vaccine against this virus is now part of the childhood immunisation programme in New Zealand. Meningitis is inflammation of the protective membranes covering the brain and spinal cord (the meninges), and can be caused by a host of different bacteria and viruses. In this case, the meningitis could have been caused by the Salmonella infection.

It’s possible that the mention of rotavirus and adenovirus are red herrings. They could have been viruses picked up by the tests but that weren’t actually causing any symptoms (perhaps being shed by the baby after previously being infected). Alternatively, the baby could have caught these infections after the Salmonellosis because of his weakened immune system.

So was it the shopping trolley?!

Maybe, maybe not. The mother is adamant that after ruling everything out, it must have been the shopping trolley that was the source of her son’s illness, but in reality, people are very bad at remembering important things like what they have eaten and who they have been in contact with. The Salmonellosis could just have easily been caught by contact with an infected but asymptomatic person or animal, or their poop. But it is not beyond the realms of possibility that the trolley seat/handle was contaminated with traces of Salmonella-containing bird poop, or the poop of a previous occupant.

Searching the medical literature I was able to find one study that has looked at bacteria contamination of shopping baskets (1). Carried out in Japan, the authors grew 56 isolates of Staphylococcus aureus from 760 shopping basket handles. But it’s not just shopping baskets. There have also been plenty of studies showing just how “contaminated” our whole environment is. For example, a study of over 1000 surfaces from a range of environments, including shops, airports, restaurants and offices, found that 5-10% of the surfaces tested positive for coliforms, the bacteria associated with poop (2). Interestingly, the authors identified children’s playground equipment as a priority for more research into potential exposure to infectious diseases.

While this case has clearly been awful for the family involved, its likely to be a fairly rare event, so I’m not sure we should all become terrified of shopping trolleys as a result. In reality, bacteria and viruses are EVERYWHERE. Rather than attempting to decontaminate every surface we touch (and its not clear how effective a quick once over with a disinfectant wipe actually is…), the best way to avoid diseases like Salmonellosis is to practice good hand hygiene, admittedly a tall order for young kids.

*Earlier this year, hundreds of people in Australia became infected after eating contaminated pre-packaged salad.

A virus is essentially an information system (encoded in DNA or RNA) surrounded by a protective coat and shaped by evolution to ensure its own replication and survival.

Viruses grow only in living cells. But they infect everything from the simplest, single-cell organisms, such as amoebae, to multicellular, multi-organ ecosystems like us.

Bacteria, on the other hand, are cells in their own right and carry all the molecular machinery needed for their reproduction. As a consequence, they have unique biochemical pathways that can be targeted by broad-spectrum antibiotics.

Antiviral drugs tend to be unique for the particular virus, or closely related family of viruses. This has made them much less available than antibacterial drugs.

Tracing our molecular history

Evidence of our long history of infection is found in ancient fragments of viral DNA that have passed from mother to foetus. These are not known to cause problems and may even be of some benefit.

Every human also has a “virome” of persistent pathogens they’ve contracted since birth. Herpes simplex type 1 (which causes cold sores), Epstein Barr virus (which causes glandular fever or “kissing disease” in adolescents) and cytomegalovirus (also a member of the herpes family), for instance, stay with us for life.

Gene sequence analysis allows us to infer how long Homo sapiens has been associated with particular viruses. There is evidence, for example, that lineages of human T cell leukemia virus type 1 (HTLV1), a virus that grows only in us to cause leukemia and other diseases, has been around for many thousands of years.

The original Australians carry two “strains” of HTLV1 that are thought to have diverged more than 9,000 years back and which are a significant and under-recognised cause of illness in some Indigenous communities.

Piecing together the rest

Humans have a deep history of viral infections, but other than the molecular analysis of current or recently circulating pathogens, the data is fragmentary.

That may change as researchers probe more ancient DNA from Egyptian mummies, where there is evidence of lethal tuberculosis and malaria (neither of which is viral) dating 1,500 to 4,000 years back. The evidence so far suggests mummies suffered from smallpox and polio.

With recorded history, we are limited to much more recent accounts. From 430-427 BCE, the Plague of Athens, described by Thucydides, killed more than one-third of the population. The cause is unknown, though the favoured candidate is the bacterial infection typhus.

Then the Antonine plague (165-180 CE), also called the Galenic plague after the great Roman physician, was likely viral, with smallpox being the probable cause.

Chinese paediatrician Wan Quan (1495-1585) identified smallpox and, around that time, the Chinese began the process of “immunising” healthy subjects by blowing powdered smallpox scab material up the nose.

Recognisable descriptions of influenza outbreaks date back to 1580, with three such events during each of the 19th and 20th centuries.

Setting aside HIV/AIDS, which may be regarded as a “continuing” (since 1981) pandemic, the worst pandemic of modern times was the 1918/19 Spanish flu that killed 40-50 million people globally. Spain gets a bad rap for this: the virus had been active in the trenches on the western front for months, but neither set of combatants wanted to admit their armies were being weakened.

We don’t know if a milder variant of this virus was circulating in France the previous year, or if the pandemic strain was brought across to France in US troop ships after “taking off” in the crowded conditions of army recruit camps.

The 1918/19 H1N1 flu likely “jumped” from birds to people (or via pigs), while the much less virulent 2009 H1N1 strain clearly originated in pigs to cause the first human pandemic of the 21st century. Mass air travel ensured that it was around the planet in six months.

The 2009 virus retains 1918 genes that were maintained for more than 90 years in pig populations. Way back in 1917/18, did pigs transmit the original H1N1 pandemic flu to us, or did we pass it to them? Either could be the case.

Swine flu was around the world in six months. Ka-ho Pang/Flickr, CC BY-NC-ND

Similarly, the human immunodeficiency virus type 1 (HIV1), the most prominent cause of the human acquired immune deficiency syndrome (AIDS), is thought to have “jumped” to humans back in the first half of the 20th century, perhaps when a hunter cut his hand while killing an infected chimpanzee (bush meat).

Then, as often occurs, HIV1 seemed to spread slowly between people until, in 1981, we saw the dramatic emergence of AIDS in New York and San Francisco.

Many and varied factors influence such disease incursions from other species, then “breakouts” from small, localised events. Changes in social practices, patterns of international travel and the movement of humans (with increasing population size) into previously forested areas are obvious triggers.

It’s not just humans

We are not, of course, the only species that can suddenly acquire infections from other vertebrates. Canine distemper virus (CDV) has, for instance, become established in Serengeti spotted hyenas.

Regular, fatal outbreaks in lions look to have come directly from dogs or perhaps other wildlife, including hyenas.

CDV is related to both bovine rinderpest virus (dubbed cattle plague) and human measles, both of which are closer to each other. Gene sequences suggests these two pathogens diverged about 1,000 years back, perhaps from an ancestral virus that is not identical to either.

Eradicating viruses with vaccinations

Using vaccination and other disease control measures, we have eliminated two virus infections that have, through the ages, caused massive economic damage and loss of life: human smallpox (1980) and bovine rinderpest (2011).

Another scourge, polio, is close to eradication. But problems remain with vaccine coverage (and the safety of the medical teams) in regions that are essentially war zones.

Thanks to an oral vaccination, polio is close to being eradicated. PROSanofi Pasteur/Flickr, CC BY-NC-ND

We could also eradicate measles, but this is hampered by some parents in the developed world who believe they do not have a responsibility to immunise their children against the standard infections of childhood.

These three rare conditions all cause damage to the nervous system, which includes the brain, spinal cord and nerves. Our nervous system functions to send signals throughout the body to co-ordinate movement, sense our environment and regulate body function.

What is acute disseminated encephalomyelitis (ADEM)?

ADEM is a rare autoimmune disease that causes lesions in the brain and spinal cord. Disease is usually triggered by a previous infection or vaccination, although why this occurs is not well understood. For example, one in 1,000 people infected with measles goes on to develop ADEM. Rates of disease have decreased in developed countries, due to reduced rates of infection.

Immune cells normally protect our body against disease, by killing invading viruses and bacteria. In ADEM, these immune cells attack our nerves within the brain and spinal cord and cause damage. Damage destroys the insulating coating on our nerve cells, called myelin, and interferes with signalling in the nervous system.

Early symptoms include fever, low energy, headache nausea and vomiting. Within several days, symptoms escalate and can range from low energy to coma, with weakness along one side of the body or in the legs (hemiparesis/paraparesis). Symptoms can also include loss of control of body movements (ataxia) and other movement disorders. Anti-inflammatory drugs are usually used to try to reduce damage.

Symptoms can start to improve quickly (within days) and people usually fully recover within six months. Most people experience no long-term symptoms. However, some individuals do “relapse”, meaning they go on to experience another round of symptoms.

If patients continue to having recurring symptoms, they may be diagnosed with multiple sclerosis. Multiple sclerosis causes similar damage and symptoms to ADEM and is a life-long disease. It is currently unclear whether ADEM leads to multiple sclerosis in some people or whether ADEM is simply confused for the first episode of multiple sclerosis.

How do you show Zika causes neurological disease?

Last week, the Centers for Disease Control and Prevention (CDC) concluded that Zika infection causes microcephaly. Microcephaly is a birth defect that causes abnormally small head size in infants and is associated with brain defects.

CDC researchers have also provided evidence for a strong link between Zika infection and Guillain-Barre syndrome. Guillain-Barre syndrome, which causes temporary paralysis and can lead to death, has increased in 12 countries currently experiencing a Zika virus outbreak.

Demonstrating Zika infection actually causes disease requires extensive study and consideration of a range of data. This was done in the recent publication connecting Zika infection and microcephaly. These conclusions required data showing individuals who develop disease are infected with Zika, as well as population data showing that rates of disease increased in Zika-affected areas and ruling out other possible causes.

The conclusions were also supported by laboratory data demonstrating that Zika virus can infect and kill nerve cells. These functional studies in the lab provide a logical connection between Zika virus and neurological disease.

Is ADEM linked to Zika virus infection?

A possible link between Zika infection and ADEM has been proposed based on recent study findings from Brazil. In 151 patients with confirmed arbovirus infection (a group of viruses that includes Zika), six developed neurological symptoms.

All six patients were infected by Zika virus and four developed Guillain-Barre syndrome. The remaining two developed ADEM. ADEM is well known to develop after infection by a range of viruses, so it’s entirely possible Zika virus will be added to this list. However, it should be noted that even among people infected with Zika virus, a very small number will develop ADEM.

While a link between Zika infection and ADEM is cause for concern, it remains to be formally proven. It may take months or years of study to confirm whether Zika actually causes ADEM. The hope is that through continued study we can better understand both Zika infection and ADEM disease and develop better ways of treating both.

]]>https://sciblogs.co.nz/guestwork/2016/04/21/explainer-autoimmune-disorder-newly-linked-zika/feed/0An update on Zika infection and pregnancyhttps://sciblogs.co.nz/infectious-thoughts/2016/03/16/zika-and-microcephaly-the-latest-data/
https://sciblogs.co.nz/infectious-thoughts/2016/03/16/zika-and-microcephaly-the-latest-data/#respondWed, 16 Mar 2016 02:02:19 +0000https://sciblogs.co.nz/?p=226008New research which looked at the data from the 2013-2014 outbreak of Zika in French Polynesia, estimates that the risk of microcephaly is about 1 for every 100 women infected with the Zika virus during the first trimester of pregnancy.

Zika is the virus spread by mosquitoes (and more rarely by sexual transmission) that is currently causing concern in over 30 countries and territories across the Americas and Pacific because of a potential link between infection during pregnancy and babies being born with smaller heads and brains (known as microcephaly). The last few weeks has seen a flurry of papers and reports strengthening that link. Now a paper has been published in the journal The Lancet which looks back at data from a previous outbreak of Zika, which happened in French Polynesia (1). The outbreak began in October 2013, peaking in December and ending the following April. More than 31,000 people visited their doctor with suspected Zika virus infection. During the outbreak, 8 cases of microcephaly were identified, 7 of them during a four month period around the end of the outbreak. Five of the 8 pregnancies were terminated.

Using researchers built a mathematical model to estimate the expected number of microcephaly cases using data on the total number of cases of microcephaly, the weekly number of doctors visits for suspected Zika virus infection, blood tests confirming the presence of Zika virus antibodies taken post-outbreak, and the total number of births during the outbreak. Using their model, the researchers were estimate that the risk of microcephaly is 95 in 10,000 women (approximately 1 in 100) infected with Zika virus in the first trimester of pregnancy. The normal risk is about 2 per 10,000.

Reference:

Cauchemez et al. Association between Zika virus and microcephaly in French Polynesia, 2013–15: a retrospective study. The Lancet. http://dx.doi.org/10.1016/S0140-6736(16)00651-6

]]>https://sciblogs.co.nz/infectious-thoughts/2016/03/16/zika-and-microcephaly-the-latest-data/feed/0Zika: a potential new mozzie vector?https://sciblogs.co.nz/infectious-thoughts/2016/03/04/zika-a-potential-new-mozzie-vector/
https://sciblogs.co.nz/infectious-thoughts/2016/03/04/zika-a-potential-new-mozzie-vector/#respondFri, 04 Mar 2016 02:40:55 +0000https://sciblogs.co.nz/?p=225461Brazilian scientists announce Zika could be spread by a different species of mosquito, one more common in Brazil and present in countries like New Zealand.

According to the US Centers for Disease Control (CDC), the Zika virus is currently known to be transmitted by Aedes species mosquitoes, namely A. aegypti and A. albopictus. Media are now reporting that Brazilian scientists say they have succeeded in infecting another mosquito species, Culex quinquefasciatus, with the Zika virus in a laboratory. The report says the researchers injected the mosquitoes with Zika-infected rabbit blood and that the virus circulated through the mosquitoes’ bodies and into their salivary glands, meaning they might be able to transmit Zika to a person when taking a blood meal. What the scientists don’t yet know is if ‘wild’ mosquitoes are carrying the virus. Similar studies will be going on with other mosquito species, as it’s important to know just how many have the potential to transmit this worrying virus.

These latest findings are a concern as the researchers say C. quinquefasciatus is 20 times more common than A. aegypti in Brazil. It also has a different lifestyle so will require a different approach to kill. According to the report, C. quinquefasciatus can survive colder temperatures and prefers to live up trees where it feeds on birds. The relevance to New Zealand is that this IS one of the 16 mosquito species found here. The Science Media Centre quotes Dr José Derraik, a Senior Research Fellow at the University of Auckland, as saying:

“So, while it is correct to say that the known mosquito vectors of Zika virus are not present in New Zealand, it is misguided (and potentially dangerous) to assume that we do not have mosquito vectors capable of transmitting the virus. Zika virus in particular, has been very poorly studied until the outbreak in Brazil, which means that we simply do not know whether the species of mosquitoes in New Zealand are able to transmit the virus to humans.”

José is absolutely right, and I apologise for my sloppy language around this!

Update: José’s written a paper about Zika in the Pacific which you can read here.

Does this finding mean Zika could establish in New Zealand?

If we have the ‘right’ species of mosquito here, for Zika to establish in New Zealand, we would need those mosquitoes to feed on a person with Zika in their bloodstream, then go on to feed on someone else, who in turn could be fed on by another of the ‘right’ species of mosquito and so on. While we still have relatively small numbers of infected travellers coming in to NZ, the risk is low, but it shows that we can’t be complacent. I think everyone who thinks they may have been exposed to Zika should take all precautions to avoid being bitten by mozzies, even here in NZ, and to make sure they use condoms to minimise the chance of passing the virus on to their partner(s) and creating more cases.

]]>https://sciblogs.co.nz/infectious-thoughts/2016/03/04/zika-a-potential-new-mozzie-vector/feed/0Zika in NZ: sexual transmission or intrepid mosquito?https://sciblogs.co.nz/infectious-thoughts/2016/03/03/zika-in-nz-sexual-transmission-or-intrepid-mosquito/
https://sciblogs.co.nz/infectious-thoughts/2016/03/03/zika-in-nz-sexual-transmission-or-intrepid-mosquito/#respondThu, 03 Mar 2016 08:50:29 +0000https://sciblogs.co.nz/?p=225415The New Zealand Ministry of Health are investigating a case of Zika in a woman who hasn’t travelled to a Zika-affected country recently. Is it a case of sexual transmission or a rogue mosquito?

Zika is a mosquito-borne virus currently infecting people in many countries in the America’s and the Pacific. The virus is causing concerns as it seems to be associated with an increase in babies being born with small brains and heads (a condition known as microcephaly).

The New Zealand Ministry of Health say they are currently investigating a case of Zika in a woman who hasn’t recently travelled to a Zika-affected country. The woman’s partner has recently returned from a country with Zika and tested positive for Zika so the Ministry say they are investigating whether the woman was infected through sexual transmission or by being bitten by an infected mosquito brought into the country in her partner’s luggage.

Rogue mosquito an unlikely scenario

As there are a few documented cases of Zika virus being transmitted sexually, and of Zika virus being present in a man’s semen after infection, I think it’s more likely that the woman was infected by her partner, rather than by being bitten by a rogue mosquito. It can’t have been just any mosquito either. It would have had to have been an infected female, as only the females bite – they need a blood meal for laying eggs.

Lots of unknowns when it comes to the sexual transmission of Zika virus

Not a lot is known about the sexual transmission of Zika virus. There have only been a few cases, and only ever from men to women. It’s not yet known if the men have to had symptoms to be infectious or how long an infected man remains infectious. It’s also not known if women can pass the virus on to men, and if Zika can be transmitted through other body fluids, like saliva.

The risk to New Zealand

However the woman was infected, the risk to New Zealand is low. If she was infected through sexual transmission, then any further cases here will be related to the number of sexual partners the infected person has. As we don’t have the right mosquitoes here, the chain of infected people is likely to end with the infected partner(s). This is because the normal route of transmission is from mosquitoes biting infected people and then going on to bite someone else. If on the other hand the woman was infected by one rogue mosquito coming in on someone’s luggage, then we might see a few cases depending on how many times the mosquito fed before it died (the mosquitoes normally only live a few weeks).

Preventing Zika infection

The advice from authorities has been clear from the beginning. The Centers for Disease Control in the US, the World Health Organisation and UK’s National Health Service all say: if you are a man who has travelled to an infected country and you have a fever or likely have Zika, you should either abstain from having sex or use a condom. This properly, repeatedly and for oral, anal and vaginal sex. What’s confusing though is that advice on how long men should wear a condom or abstain from sex for varies, from four weeks to six months. This is because it isn’t clear yet how long a man may remain infectious. Personally, I would err on the side of six months rather than four weeks.

The growing evidence of a link to microcephaly

The CDC have recently reported on Zika infection in pregnant US travellers and it makes stark reading. Between August 2015 and February 2016, the CDC received 257 requests for Zika virus testing for pregnant women. Nine women tested positive. Of these nine women, six were believed to be infected during the first trimester of their pregnancy. The report states that two of these women miscarried, two women elected to terminate their pregnancies, one women gave birth to a baby with severe microcephaly, and the sixth woman is still pregnant. Of the women infected during the later stages of pregnancy, one has given birth to an apparently healthy baby with a normal head size, while the remaining two women are still pregnant. The report describes some of the cases and they make sad reading. “Patient A” was a pregnant woman in her 30s who miscarried. What they refer to as the “products of conception” tested positive for Zika virus. “Patient B” was another woman in her 30s. Her 20 week scan revealed a foetus with severe brain abnormalities. She decided to terminate the pregnancy. What an awful end to a trip overseas.

]]>https://sciblogs.co.nz/infectious-thoughts/2016/03/03/zika-in-nz-sexual-transmission-or-intrepid-mosquito/feed/0Zika update – sexual transmission & GM mosquitoeshttps://sciblogs.co.nz/infectious-thoughts/2016/02/04/zika-update-sexual-transmission-gm-mosquitoes/
https://sciblogs.co.nz/infectious-thoughts/2016/02/04/zika-update-sexual-transmission-gm-mosquitoes/#respondWed, 03 Feb 2016 20:21:00 +0000https://sciblogs.co.nz/?p=224077Earlier this week the WHO declared the Zika virus outbreak in the Americas a Public Health Emergency of International Concern and yesterday the CDC reported that someone in Dallas had become infected with the virus by having sex with someone infected overseas. Meanwhile, the internet is awash with claims that genetically-modified mosquitoes are to blame for the outbreak in Brazil.

In case you need reminding, Zika is a virus spread by mosquitoes which is currently suspected of being responsible for a cluster of microcephaly cases – a condition in which babies are born with a small head and brain. I’ve previously posted an FAQ about Zika but here is another based on these latest developments.

What is a Public Health Emergency of International Concern?

By calling the outbreak a Public Health Emergency of International Concern, the WHO can call on a binding international agreement to fast track research and aid to tackle the infection. This is only the fourth time the WHO have made such a declaration; the first was for swine flu in 2009, the second for polio in 2014 and the last was for the Ebola outbreak in West Africa.

There are so many unanswered questions regarding Zika so this declaration will hopefully speed up the search for answers. Questions like: which species of Aedes mosquitoes can carry the virus? Is the link with microcephaly real? If so, when are pregnant women at risk and how many infected women will pass the virus to their developing baby? Do the women need to be symptomatic? Is the link with Guillain-Barré Syndrome real? How far will the virus spread? Will it be possible to develop a vaccine?

While the research gets underway, the first thing has to be to provide access to contraception and to tackle the mosquitoes. More on tackling the mosquitoes later, but there are interesting times ahead for the many women at risk of being infected with Zika in countries with almost no access to contraception and abortion.

Will the fact that Zika can be sexually transmitted mean the virus could establish itself in countries without the right mosquitoes?

I think this is the question most on people’s minds with the announcement that the CDC has confirmed that someone in Dallas became infected with Zika by having sex with someone who had caught Zika while overseas. I think its safe to say that this mode of transmission is going to play a minor role in spreading Zika. The major route of transmission is from mosquitoes feeding on infected people and then spreading it to other people when they feed again. When infected people travel to countries without the right mosquitoes, cases usually end there. Yes, the sexual transmission route could mean infected people cause small clusters of cases in countries without the mosquitoes, like this case in Dallas. The number of cases will be related to how long the virus stays in a man’s semen and how many sexual partners he has. From all indications so far, infection with the Zika virus is for a relatively short period of time so its likely that men are only infectious for a few weeks. Contrast this with HIV which causes a chronic infection where people are infectious for years without treatment. Once there are better ways to detect the virus in those who have been infected, scientists will be better able to answer questions about how many men end up with the virus in their semen and how long it stays there.

Why has the outbreak exploded in the Americas?

It’s likely this outbreak is the culmination of a perfect storm of factors. Mosquito behaviour will be part of it – with the mosquito species most involved in Brazil, the female takes a blood meal before laying a batch of eggs and can produce about five batches in her life time, spreading the virus between people with each bite. Contrast this with other species of mosquitoes that only have one big blood meal, then lay one batch of eggs. Another important factor is the number of mosquitoes around. The strong El Niño in the Pacific has caused flooding in Brazil, Paraguay and other countries. This abundance of clean water has caused a mosquito population boom. The more mosquitoes there are, the more virus will be transmitted, meaning more infected people for mosquitoes to feed on. The virus has spread to other countries in the region because the disease doesn’t really incapacitate those infected. If they travel to somewhere with the right mosquitoes and still have virus in their blood when they arrive, then the mosquitoes will pick it up and start transmitting it to other people when the mosquitoes feed.

Whats all this about genetically modified mosquitoes in Brazil?

One of the best defenses against Zika is going to be control of the mosquito population. Over the last few years Brazil has been trialing the use of genetically-modified mosquitoes to control cases of Dengue fever, another viral infection spread by the same mosquito. The GM mosquitoes are a high tech version of a well established technique called the sterile insect technique. The usual way to do this is to irradiate a population of male mosquitoes in the lab so they become sterile and then release them into the environment in huge numbers to outcompete the fertile males for breeding females. This way the mosquito population crashes as less offspring are born. The problem with the irradiation technique is that it can affect more than just a male mosquito’s fertility. It can also affect their overall ‘fitness’ – their ability to survive in the environment and compete with normal males.

A company called Oxitec have used genetic engineering as a smarter way to make male Aedes mosquitoes for the sterile insect technique and they’ve been trialing them in Brazil over the last few years. Cue maps showing the sites where the mosquitoes are being trialed overlapping with the epicentre of the outbreak (they don’t) and cries that the GM males being released are spreading the virus (they can’t – male mosquitoes don’t bite!). Pure anti-GM propaganda. There is a great take down of all the claims here.

]]>https://sciblogs.co.nz/infectious-thoughts/2016/02/04/zika-update-sexual-transmission-gm-mosquitoes/feed/0Zika virus: an FAQhttps://sciblogs.co.nz/infectious-thoughts/2016/01/26/zika-virus-an-faq/
https://sciblogs.co.nz/infectious-thoughts/2016/01/26/zika-virus-an-faq/#respondMon, 25 Jan 2016 22:30:18 +0000https://sciblogs.co.nz/?p=223673A virus spread by mosquitoes and which has been linked to babies being born with smaller heads and brains in Brazil is making the news. Here’s a quick FAQ to bring you up to speed.

What is Zika and where has it come from?

Zika is an RNA virus that was first identified in monkeys in Uganda in 1947. The first human cases were reported in 1952 in Uganda and Tanzania. There were only a small number of reported cases after that, until the first documented outbreak in Yap in Micronesia in 2007. There was another outbreak in the Pacific in 2013. From the Pacific, Zika seems to have spread to the Americas via Easter Island, appearing in Brazil in April 2015. There is some mention online that Zika might have entered Brazil during the FIFA World Cup in 2014. Since April 2015, it’s estimated that between 440,000 to 1.3 million people in Brazil have been infected with the virus. The World Health Organisation (WHO) now lists Zika virus also present and locally transmitting in Barbados, Bolivia, Colombia, Dominican Republic, Ecuador, El Salvador, French Guiana, Guadeloupe, Guatemala, Guyana, Haiti, Honduras, Martinique, Mexico, Panama, Paraguay, Puerto Rico, Saint Martin, Suriname and Venezuela.

Update: Just found this reference that suggests entry of Zika to Brazil was via the Va’a World Sprint Championship canoe race, in which four Pacific countries, which had cases of Zika during the 2013/2014 outbreak, competed.

How is Zika virus transmitted?

The Zika virus is mainly transmitted to people by mosquito bite, although there are some reports of sexual transmission through the semen of infected men. Mosquitoes of the Aedes family are the culprits here. They can also transmit other viruses, including West Nile virus, Dengue and Chikungunya, but not the malaria parasite. That’s a different mosquito. Adult Aedes mosquitoes can live for 2-4 weeks depending on the environmental conditions. Female Aedes mosquitoes are daytime feeders; after taking a blood meal, a female will produce on average 100 to 200 eggs, depending on the size of the blood meal. A female Aedes mosquito can produce up to five batches of eggs during her lifetime. The female mosquitoes pick up the Zika virus when feeding on an infected person, and then go on to transmit the virus to other people when they feed again.

What are the symptoms of Zika infection?

Until recently, the Zika virus was thought to give people a mild infection. About 2-7 days after a mosquito bite, 1 in 4 people develop symptoms which could include a mild fever, conjunctivitis, a headache, joint pain and a rash. But since October 2015, there have been over 3,500 babies born in Brazil with microcephaly – a quite uncommon complication of pregnancy in which babies brains don’t develop properly and they are born with a smaller head and brain. Microcephaly can cause convulsions, difficulty feeding and developmental delays. The rise in the number of cases correlates with the rise in cases of Zika infection in the general population. Researchers have also isolated Zika RNA from the placenta of a woman with a foetus with microcephaly, suggesting the virus can cross the placental barrier, and the amniotic fluid of two other pregnant women whose foetuses were diagnosed with microcephaly by ultrasound (1). The virus was also found in the blood and tissues of a newborn that died of microcephaly. It’s thought that women who are infected with the virus during early pregnancy are most at risk of transmitting it their developing baby.

The WHO is also investigating an increase of Guillain-Barré Syndrome (GBS) cases in El Salvador. GBS is an autoimmune disease caused by the body’s immune system mistakenly attacking the peripheral nerve. Symptoms include numbness, tingling, and pain, muscle weakness and, in severe cases, trouble breathing. The average number of GBS cases a year is usually 169, but in between the 1st December 2015 and the 6th January 2016, El Salvador reported 46 GBS cases, including 2 deaths.

What’s the treatment for Zika?

There is currently no treatment or vaccine for Zika. The main way to avoid infection is to prevent being bitten by mosquitoes and to try to stop Aedes mosquitoes breeding. Women in outbreak countries are currently being advised to delay getting pregnant.

How far is Zika going to spread?

One of the main ways Zika has spread is when infected people have traveled and been fed on by local Aedes mosquitoes, which then go on to infect other people. Bogoch and colleagues have made a model of where Zika might go next based on people leaving Brazilian airports. Their paper has just been published in the Lancet (2). Between September, 2014, and August, 2015, 9·9 million travellers departed from Brazilian airports for international destinations. The majority of these (65%) travelled to the Americas, while 27% travelled to Europe and 5% to Asia. The model suggests that Argentina, Italy, and some parts of the USA could start seeing seasonal transmission of Zika virus, while over 70 million people are living in the parts of Mexico, Colombia, and the USA that could see year round transmission of the virus. The fact that Brazil is set to host the summer Olympic Games in August this year is starting to worry some people.

What’s the risk to NZ?

According to the Ministry of Health website, we don’t have the right mosquitoes in New Zealand for the Zika virus to flourish here. The main risk to New Zealanders is travelling to countries with widespread Zika transmission. This list of countries seems to be growing by the day, but most relevant to New Zealanders is probably Samoa. The CDC is advising women who are pregnant, or trying to get pregnant, to postpone travelling to countries with Zika, and if this can’t be done, to take all precautions to avoid being bitten by mosquitoes. This means using mosquito nets, covering up arms and legs with long clothing, and using proper insect repellents that contain DEET or picaridin. Now is not the time to be relying on ‘chemical-free’/homeopathic repellents or nonsense vitamin B patches.

]]>https://sciblogs.co.nz/infectious-thoughts/2016/01/26/zika-virus-an-faq/feed/0Surviving the flupocalypse!https://sciblogs.co.nz/infectious-thoughts/2015/09/07/surviving-the-flupocalypse/
https://sciblogs.co.nz/infectious-thoughts/2015/09/07/surviving-the-flupocalypse/#respondMon, 07 Sep 2015 09:35:01 +0000https://sciblogs.co.nz/?p=218755Picture this. A new virus, Mortenza, is sweeping around the world, killing millions. Despite all efforts, Mortenza reaches New Zealand and rapidly spreads around the country. In desperation, the Government isolates the tiny uninfected island of Great Barrier. How would this small community cope? Would they survive the pandemic?

This is the fascinating scenario I’ll be exploring this coming weekend in an exciting event being held on Great Barrier Island and organised by the island’s Awana Rural Women. I’ve been tasked with moderating a panel of experts to explore just how likely a scenario like Mortenza is, and what would happen if it did. How would the people of Great Barrier keep law and order? How would they stop people trying to get onto the island? And what would happen if their only doctor died?

While Mortenza may sound far-fetched, the scenario itself is a great opportunity for the 900 people living on Great Barrier Island to think about how they can better prepare themselves and their families and neighbours for any emergency or natural disaster, which was the reason Awana Rural Women president Gendie Somerville-Ryan decided to organise the event. In fact, it’s a great opportunity for all of us to think about what we would do in an emergency. First stop: a visit to the Get Ready, Get Thru website!

You can listen to Kathryn Ryan’s interview with Gendie on Radio New Zealand here or click play below.

The panelists

To discuss the scenario and answer all the community’s pressing questions, I’m joined by four panellists: a virologist, a civil defence expert, a social scientist specialising in crisis decision making and a science fiction writer.

Associate Professor Lance Jennings is a clinical virologist at Canterbury District Health Board and director of New Zealand’s WHO National Measles Laboratory. Lance has been instrumental in the development of flu control strategies for New Zealand, including the introduction of free vaccines and pandemic planning. Who better to pull out the facts from the fiction in the Mortenza scenario!

John Titmus, of the Ministry of Civil Defence and Emergency Management, is the Northern Regional Coordinator responsible for supporting the four northern Civil Defence Emergency Management Groups. A former member of the Royal New Zealand Navy, John is part of a team which leads disaster management capability building in the Pacific and led the United Nations Disaster Assessment and Coordination Teams into Sri Lanka during the Boxing day Tsunami and into Louisiana USA during Hurricane Katrina.

Professor David Johnston is a Senior Scientist at GNS Science and director of the Joint Centre for Disaster Research in the School of Psychology at Massey University. His research focuses on human responses to volcano, tsunami, earthquake and weather warnings, crisis decision-making and the role of public education and participation in building community resilience and recovery.

Karen Healey is a teacher and the author of the young adult fantasy novels Guardian of the Dead and The Shattering, which are set in contemporary New Zealand, the science fiction duology When We Wake and While We Run, set in a future Australia, and several short stories. Karen’s books have been variously awarded an Aurealis Award, a Sir Julius Vogel Award, several Storyline Notable Book most recently, the NZ Post Teen Choice Award. They have been finalists for the Cybils, the Inkys, the NZ Post Children’s Book Awards, the LIANZA awards, and the William C. Morris Debut Book Award, and regularly feature on best-of-the-year book lists.